Nrf2 Signaling and the Slowed Aging Phenotype: Evidence from Long-Lived Models

Figure 2

Nrf2 regulated protein expression in skeletal muscle from mice chronically fed with rapamycin. Nrf2, NQO1, and SOD-1 were significantly greater in skeletal muscle from male rapamycin (Rap.) treated mice. Chronic rapamycin feeding suppressed Prdx1 expression compared to controls. Nrf2, NQO1, SOD-1, and Prdx1 were analyzed by western blotting and normalized to tubulin, shown below the proteins from each blot. Data are expressed as a ratio of target protein to tubulin (mean ± SEM). males and females in each condition. UM-HET3 mice were generated by the offspring of crosses between (BALB/cByJ x C57BL/6J) F1 females and (C3H/HeJ x DBA/2J) F1 males. Mice were fed with chow mixed with encapsulated rapamycin at 14 mg/kg food (equivalent to 2.24 mg of rapamycin/kg body weight/day) or normal chow for 12 weeks in accordance with the original study describing lifespan extension [6].